GRP78在食管癌细胞ECA-109增殖过程中的功能研究

Study the Function of GRP78 in Cell Proliferation Process in Esophageal Cancer Cell Line ECA-109

食管癌在中国是高发性肿瘤,并具有较高的致死率。肿瘤细胞的持续增殖与细胞增殖失调密切相关。肿瘤细胞在增殖过程中需要合成大量蛋白质,葡萄糖调节蛋白78(glucose regulatedprotein,GRP78)作为分子伴侣,在蛋白质的折叠、组装、修饰和错误折叠蛋白的降解过程中发挥着重要作用。该研究通过构建pGRP78-EGFP-N1重组质粒,瞬时转染ECA-109细胞,研究GRP78过表达对细胞增殖能力的影响;采用RNA干扰技术,瞬时转染靶向GRP78的siRNA,研究敲低GRP78对细胞增殖能力的影响。该研究发现GRP78过表达后,更多的细胞从G1期进入S期和G2/M期,细胞增殖速率加快,细胞克隆形成率亦明显提高;敲低GRP78后,细胞更多地被阻滞在G1期而无法进入S期和G2/M期,细胞增殖速率减慢,细胞克隆形成率降低。GRP78可能通过调节细胞周期而促进ECA-109细胞的增殖。

In China, esophageal cancer is a malignant tumor of high incidence and high mortality. Sus- tained proliferation of tumor cells is closely related to the cell proliferation disorder. Large amounts of proteins need to be synthesized during tumor cell proliferation process. GRP78 as a molecular chaperone, plays an important role in the process of protein folding, assembly, modification and misfolded protein degradation. The research studied the influence of proliferation ability with over-expression or knock-down of GRP78 in ECA-109 cells through tran- sient transfection of GRP78 recombinant plasmid pGRP78-EGFP-N1 or siRNA, respectively. The study found that after GRP78 over-expression, more cells converted from GI phage to S and GE/M phages, then cell proliferation rate and cell clony formation rate were increased; as well as after knock-down GRP78, more cells were arrested in G~ phage and couldn＇t transfer into S and GE/M phages, then cell proliferation rate and cell clony formation rate werereduced. GRP78 may promote ECA-109 cell proliferation by regulating the cell cycle.